Activation of anaplastic lymphoma kinase (ALK) through chromosome rearrangement, amplification, mutation or deregulated expression has been found in anaplastic large cell lymphomas, inflammatory myofibroblastic tumors, rhabdomyosarcomas, non-small cell lung cancers (NSCLC), glioblastomas, neuroblastomas, ...
Activation of anaplastic lymphoma kinase (ALK) through chromosome rearrangement, amplification, mutation or deregulated expression has been found in anaplastic large cell lymphomas, inflammatory myofibroblastic tumors, rhabdomyosarcomas, non-small cell lung cancers (NSCLC), glioblastomas, neuroblastomas, breast cancers and others. Although preclinical studies with ALK inhibitors (small molecules, siRNAs and selective ribozymes) have yielded promising data, only a few of the inhibitors reached clinical trials. Crizotinib, a c-Met and ALK inhibitor, has recently demonstrated high objective response rates in ALK-positive NSCLC patients but resistance seems inescapable. We propose to launch a Research Topic under Frontiers in Cancer Molecular Targets and Therapeutics to address questions related to ALK signaling in cancer, mechanisms of ALK inhibitor action and resistance, development and characterization of next generation inhibitors against ALK, its downstream molecules and ligands, novel technologies for ALK rearrangement detection, and innovative strategies for target-specific treatment of ALK-positive cancer patients. Basic, translational, clinical research papers and reviews are all welcome.
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